CaMKII is involved in cardiac hypertrophy and apoptosis induced by Iso and testosterone (Bin-Dayel et al., 2016; Duran et al., 2017; Park et al., 2018), and at the epigenetic level, CaMKII inactivates the negative regulator of adverse cardiac remodeling histone deacetylase 4 (HDAC4), leading to transcriptional activation of the myocyte enhancer factor 2 (MEF2), and phosphorylates histone H3 (Backs et al., 2009; Awad et al., 2013). This evidence concerns the gene HDAC4 and cardiac hypertrophy.